Increased protein intake, at the expense of maltodextrin, lowers BP in overweight adults with upper-range prehypertension and grade 1 hypertension. This trial was registered at www.trialregister.nl as NTR 1362.

The replacement of dietary carbohydrates with proteins can lower blood pressure (BP), but the mechanisms remain unclear. This randomized, double-blind, parallel-group study aimed to compare 12-h postprandial sympathetic and hemodynamic responses after high-protein (HP) meals and high-carbohydrate (HC) meals. Fifty-two men and women with untreated elevated BP were tested on d 1 and after 4 wk of supplementation [3 × 20 g protein (HP) or maltodextrin (HC) per day]. No between-group differences were found in postprandial plasma norepinephrine on d 1 and at wk 4. On d 1, postprandial mean arterial pressure (MAP) decreased more in the HC group than in the HP group (P = 0.002). This difference was not present at 4 wk, because the postprandial decline in MAP tended to become larger in the HP group after 4 wk of supplementation (P = 0.07). On both test days, postprandial total peripheral resistance tended to decrease more in the HC group (P < 0.08). After 4 wk of supplementation, cardiac output tended to increase more in the HC group (P = 0.08). In conclusion, ingestion of an HP diet induced a smaller decrease in BP on d 1 than did ingestion of an HC diet. This difference disappeared after 4 wk due to a more pronounced decrease in BP in the HP group after 4 wk than on d 1. These findings cannot explain the BP-lowering effect ascribed to dietary proteins.

Diet composition may affect blood pressure (BP), but the mechanisms are unclear. The aim of the present study was to compare postprandial BP-related responses to the ingestion of pea protein, milk protein and egg-white protein. In addition, postprandial BP-related responses to the ingestion of maltodextrin were compared with those to the ingestion of sucrose and a protein mix. We hypothesised that lower postprandial total peripheral resistance (TPR) and BP levels would be accompanied by higher plasma concentrations of nitric oxide, insulin, glucagon-like peptide 1 (GLP-1) and glucagon. On separate occasions, six meals were tested in a randomised order in forty-eight overweight or obese adults with untreated elevated BP. Postprandial responses of TPR, BP and plasma concentrations of insulin, glucagon, GLP-1 and nitrite, nitroso compounds (RXNO) and S-nitrosothiols (NO x ) were measured for 4 h. No differences were observed in TPR responses. Postprandial BP levels were higher after the ingestion of the egg-white-protein meal than after that of meals containing the other two proteins (P#0·01). The ingestion of the pea-protein meal induced the highest NO x response (P#0·006). Insulin and glucagon concentrations were lowest after the ingestion of the egg-white-protein meal (P# 0·009). Postprandial BP levels were lower after the ingestion of the maltodextrin meal than after that of the protein mix and sucrose meals (P#0·004), while postprandial insulin concentrations were higher after the ingestion of the maltodextrin meal than after that of the sucrose and protein mix meals after 1 -2 h (P#0·0001). Postprandial NO x , GLP-1 and glucagon concentrations were lower after the ingestion of the maltodextrin meal than after that of the protein mix meal (P#0·008). In conclusion, different protein and carbohydrate sources induce different postprandial BP-related responses, which may be important for BP management. Lower postprandial BP levels are not necessarily accompanied by higher NO x , insulin, glucagon or GLP-1 responses.

Endothelial dysfunction (ED) and low-grade inflammation (LGI) have a role in the development of CVD. The two studies reported here explored the effects of dietary proteins and carbohydrates on markers of ED and LGI in overweight/obese individuals with untreated elevated blood pressure. In the first study, fifty-two participants consumed a protein mix or maltodextrin (3 × 20 g/d) for 4 weeks. Fasting levels and 12 h postprandial responses of markers of ED (soluble intercellular adhesion molecule 1 (sICAM), soluble vascular cell adhesion molecule 1 (sVCAM), soluble endothelial selectin and von Willebrand factor) and markers of LGI (serum amyloid A, C-reactive protein and sICAM) were evaluated before and after intervention. Biomarkers were also combined into mean Z-scores of ED and LGI. The second study compared 4 h postprandial responses of ED and LGI markers in forty-eight participants after ingestion of 0·6 g/kg pea protein, milk protein and egg-white protein. In addition, postprandial responses after maltodextrin intake were compared with a protein mix and sucrose. The first study showed significantly lower fasting ED Z-scores and sICAM after 4 weeks on the high-protein diet (P ≤ 0·02). The postprandial studies found no clear differences of ED and LGI between test meals. However, postprandial sVCAM decreased more after the protein mix compared with maltodextrin in both studies (P ≤ 0·04). In conclusion, dietary protein is beneficial for fasting ED, but not for fasting LGI, after 4 weeks of supplementation. On the basis of Z-scores, postprandial ED and LGI were not differentially affected by protein sources or carbohydrates.